FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2005898984> ?p ?o ?g. }

• W2005898984 endingPage "682" @default.
• W2005898984 startingPage "674" @default.
• W2005898984 abstract "Tumor necrosis factor alpha (TNFα) induces necroptosis and autophagy; however, the detailed molecular mechanism is not fully understood. In this study, we found that TNFα administration caused mitochondrial dysfunction and reactive oxygen species (ROS) production, which led to necroptosis and autophagy in murine fibrosarcoma L929 cells. Notably, the RIP1 (serine–threonine kinase receptor-interacting protein 1, a main adaptor protein of necroptosis) specific inhibitor necrostatin-1 (Nec-1) recovered mitochondrial dysfunction and ROS production due to TNFα administration. Moreover, pan-caspase inhibitor z-VAD-fmk (zVAD) increased RIP1 expression and exacerbated TNFα-induced mitochondrial dysfunction and ROS production, indicating that RIP1 led to mitochondrial dysfunction and ROS production. In addition, cytochrome c release from mitochondria was accompanied with TNFα administration, and Nec-1 blocked the release of cytochrome c upon TNFα administration, while zVAD enhanced the release. These further suggested that RIP1 induced mitochondrial dysfunction accompanied with cytochrome c release. Furthermore, autophagy inhibitor 3-methyladenine (3MA) did not affect RIP1 expression as well as mitochondrial dysfunction and ROS production. Together with our previous publication that autophagy was a downstream consequence of necroptosis, we concluded that TNFα induced mitochondrial dysfunction accompanied with ROS production and cytochrome c release via RIP1, leading to necroptosis and resulting autophagic cell death." @default.
• W2005898984 created "2016-06-24" @default.
• W2005898984 creator A5015928213 @default.
• W2005898984 creator A5022644338 @default.
• W2005898984 creator A5045272575 @default.
• W2005898984 creator A5075394928 @default.
• W2005898984 creator A5081451328 @default.
• W2005898984 creator A5091089849 @default.
• W2005898984 date "2012-12-01" @default.
• W2005898984 modified "2023-10-18" @default.
• W2005898984 title "RIP1-mediated mitochondrial dysfunction and ROS production contributed to tumor necrosis factor alpha-induced L929 cell necroptosis and autophagy" @default.
• W2005898984 cites W1554372630 @default.
• W2005898984 cites W1975593978 @default.
• W2005898984 cites W1977767269 @default.
• W2005898984 cites W1985538633 @default.
• W2005898984 cites W1988848002 @default.
• W2005898984 cites W2003246990 @default.
• W2005898984 cites W2004802127 @default.
• W2005898984 cites W2005928313 @default.
• W2005898984 cites W2008596036 @default.
• W2005898984 cites W2014494804 @default.
• W2005898984 cites W2020987391 @default.
• W2005898984 cites W2033955849 @default.
• W2005898984 cites W2035057964 @default.
• W2005898984 cites W2042245650 @default.
• W2005898984 cites W2052000877 @default.
• W2005898984 cites W2058160101 @default.
• W2005898984 cites W2060988288 @default.
• W2005898984 cites W2062845561 @default.
• W2005898984 cites W2062961285 @default.
• W2005898984 cites W2083578624 @default.
• W2005898984 cites W2090217381 @default.
• W2005898984 cites W2094026960 @default.
• W2005898984 cites W2099034929 @default.
• W2005898984 cites W2100142074 @default.
• W2005898984 cites W2110506515 @default.
• W2005898984 cites W2110796758 @default.
• W2005898984 cites W2120753181 @default.
• W2005898984 cites W2125457182 @default.
• W2005898984 cites W2133080613 @default.
• W2005898984 cites W2133169035 @default.
• W2005898984 cites W2139552156 @default.
• W2005898984 cites W2145206598 @default.
• W2005898984 cites W2149729174 @default.
• W2005898984 cites W2158662692 @default.
• W2005898984 cites W2161339168 @default.
• W2005898984 cites W2398664613 @default.
• W2005898984 doi "https://doi.org/10.1016/j.intimp.2012.08.003" @default.
• W2005898984 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23000518" @default.
• W2005898984 hasPublicationYear "2012" @default.
• W2005898984 type Work @default.
• W2005898984 sameAs 2005898984 @default.
• W2005898984 citedByCount "63" @default.
• W2005898984 countsByYear W20058989842013 @default.
• W2005898984 countsByYear W20058989842014 @default.
• W2005898984 countsByYear W20058989842015 @default.
• W2005898984 countsByYear W20058989842016 @default.
• W2005898984 countsByYear W20058989842017 @default.
• W2005898984 countsByYear W20058989842018 @default.
• W2005898984 countsByYear W20058989842019 @default.
• W2005898984 countsByYear W20058989842020 @default.
• W2005898984 countsByYear W20058989842021 @default.
• W2005898984 countsByYear W20058989842022 @default.
• W2005898984 countsByYear W20058989842023 @default.
• W2005898984 crossrefType "journal-article" @default.
• W2005898984 hasAuthorship W2005898984A5015928213 @default.
• W2005898984 hasAuthorship W2005898984A5022644338 @default.
• W2005898984 hasAuthorship W2005898984A5045272575 @default.
• W2005898984 hasAuthorship W2005898984A5075394928 @default.
• W2005898984 hasAuthorship W2005898984A5081451328 @default.
• W2005898984 hasAuthorship W2005898984A5091089849 @default.
• W2005898984 hasConcept C17991360 @default.
• W2005898984 hasConcept C185592680 @default.
• W2005898984 hasConcept C190283241 @default.
• W2005898984 hasConcept C203014093 @default.
• W2005898984 hasConcept C203522944 @default.
• W2005898984 hasConcept C2778175917 @default.
• W2005898984 hasConcept C28859421 @default.
• W2005898984 hasConcept C29311851 @default.
• W2005898984 hasConcept C31573885 @default.
• W2005898984 hasConcept C48349386 @default.
• W2005898984 hasConcept C55493867 @default.
• W2005898984 hasConcept C86803240 @default.
• W2005898984 hasConcept C94030615 @default.
• W2005898984 hasConcept C95444343 @default.
• W2005898984 hasConceptScore W2005898984C17991360 @default.
• W2005898984 hasConceptScore W2005898984C185592680 @default.
• W2005898984 hasConceptScore W2005898984C190283241 @default.
• W2005898984 hasConceptScore W2005898984C203014093 @default.
• W2005898984 hasConceptScore W2005898984C203522944 @default.
• W2005898984 hasConceptScore W2005898984C2778175917 @default.
• W2005898984 hasConceptScore W2005898984C28859421 @default.
• W2005898984 hasConceptScore W2005898984C29311851 @default.
• W2005898984 hasConceptScore W2005898984C31573885 @default.
• W2005898984 hasConceptScore W2005898984C48349386 @default.
• W2005898984 hasConceptScore W2005898984C55493867 @default.
• W2005898984 hasConceptScore W2005898984C86803240 @default.
• W2005898984 hasConceptScore W2005898984C94030615 @default.

• next